机构:[1]The Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, China,广东省中医院[2]Department of Clinical Education Management, The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China,[3]College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China,[4]Department of Neurology, The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China
Accumulation of beta-amyloid (A beta) causes oxidative stress, which is the major pathological mechanism in Alzheimer's disease (AD). beta-asarone could reduce A beta-induced oxidative stress and neuronal damage, but the molecular mechanism remains elusive. In this study, we used an A beta-stimulated PC12 cell model to explore the neuroprotective effects and potential mechanisms of beta-asarone. The results showed that beta-asarone could improve cell viability and weaken cell damage and apoptosis. beta-asarone could also decrease the level of ROS and MDA; increase the level of SOD, CAT, and GSH-PX; and ameliorate the mitochondrial membrane potential. Furthermore, beta-asarone could promote the expression of Nrf2 and HO-1 by upregulating the level of PI3K/Akt phosphorylation. In conclusion, beta-asarone could exert neuroprotective effects by modulating the P13K/Akt/Nrf2 signaling pathway. beta-asarone might be a promising therapy for AD.
基金:
This study was supported by the Youth Program of the National
Natural Science Foundation of China (No. 81303028) and the
Project of National Clinical Research Base (No. JDZX2015105).